Sunday, October 31, 2010

There are few food ingredients that conjure up more fear in the public mind than sugar and sugar substitutes found in manufactured products. This fear can be bolstered by a common ploy some companies and organizations use to create panic and push their products by smearing nutritive and non-nutritive sweeteners used by their competitors.

The hysteria surrounding fructose is one such example — a simple fruit sugar found in almost every natural food on the planet has been unfairly targeted as the scapegoat for all of the extra pounds on America’s waistlines.

But although it’s appropriate for people to watch for extra calories from all sources, including sugars, reasonable amounts of fructose each day as part of a balanced diet is not really anything to worry about.

What’s alarming is the attacks on fructose have become so frequent that people have started to believe that the sugar is inherently harmful to health. The hype has even led people to believe they must reduce their intake of fruit and vegetables — now that’s frightening!

It's time to put a stop to the demonizing and scare tactics.

But wait a sec… isn't it true that high-fructose corn syrup (containing 55 percent fructose, 45 percent glucose) is a cheap sugar source widely available in sodas and processed foods, and is uniquely responsible for causing the obesity epidemic?

No, not at all. The initial study that posed this hypothesis has been largely discredited. According to the nutrition science experts, there is no evidence that overconsumption of a single nutrient, such as fructose from high-fructose corn syrup, has led people to gain more weight than other foods (1,2).

The fact is Americans live in a toxic, stressful environment, overeat everything and simply do not exercise enough.

Additionally, in 2009, a supplement in the Journal of Nutrition in 2009 called for a stop to the demonization of fructose and high-fructose corn syrup (HFCS) (1). They wrote, "Evidence is presented that HFCS does not pose a unique dietary risk in healthy individuals or diabetics."

In fact, in the same paper, the author seeks to dispel other myths about fructose by pointing out the following facts:

- Fructose coexists with glucose in all common nutritive sweeteners including honey, fruits and vegetables, agave nectar, and regular table sugar (50 percent fructose, 50 percent glucose) - The human body is well adapted to handling sugars in normal ranges - Replacing all the fructose in manufactured foods with other nutritive sweeteners would not improve health or solve the obesity crisis

There is also a list of good reasons for why people should continue to have fructose in their diets.- Fructose is sweeter than glucose, so a balance of both helps food manufacturers use less sugar overall in foods.- Since fructose is absorbed differently than glucose, it blunts a glycemic response, leading to lower insulin levels. - Fructose makes things with naturally unpleasant flavors (like vitamins and minerals) taste better. Unlike non-caloric, artificial sweeteners, fructose helps to fuel the body with energy.

Eating fructose in normal ranges daily, as part of a nutritionally balanced diet, shouldn't haunt you or your waistline. As long as you’re not getting too much fructose, or any other added sugar, or using added sugars to replace nutrient-dense foods (2, 3), then there’s nothing to fear.

So, what of the scare tactics and supposed experts saying we need to limit fructose to only a few grams daily to avoid overproduction of fats in the blood and obesity? These claims are totally, utterly, unfounded.

The truth is that fructose is metabolized in the liver and is first used to replenish liver glycogen stores, which are in turn used to fuel the body during fasting. The average human liver has the capacity to store around 85 to 100 grams or more of liver glycogen.

When fructose is consumed in a normal range as our hunter-gatherer ancestors did when they ate fruits and vegetables all year round – and as part of a reduced-calorie diet for building muscle and losing weight – it and its cousin sweeteners such as sucrose, glucose, honey, agave nectar, fruit juice concentrates, and sugar alcohols really aren’t so freaky after all.

Monday, October 25, 2010

When it comes to losing fat and maintaining muscle, at the same time, there are no shortcuts. The process generally has to be slow to be healthy. When one loses a lot of weight in a few days, most of what is being lost is water, followed by carbohydrates. (Carbohydrates are stored as liver and muscle glycogen.) Smaller amounts of fat and protein are also lost. The figure below, from Wilmore et al. (2007), shows the weights in grams of stored water, carbohydrates (glycogen), fat, and protein lost during a 30-day water fast.

On the first few days of the fast a massive amount of water is lost, even though drinking water is allowed in this type of fast. A significant amount of glycogen is lost as well. This is no surprise. About 2.6 g of water are lost for each 1 g of glycogen lost. That is, water is stored by the body proportionally to the amount of glycogen stored. People who do strength training on a regular basis tend to store more glycogen, particular in muscle tissue; this is a compensatory adaptation. Those folks also tend to store more water.

Not many people will try a 30-day fast. Still, the figure above has implications for almost everybody.

One implication is that if you use a bioimpedance scale to measure your body fat, you can bet that it will give you fairly misleading results if your glycogen stores are depleted. Your body fat percentage will be overestimated, because water and glycogen are lean body mass. This will happen with low carbohydrate dieters who regularly engage in intense physical exercise, aerobic or anaerobic. The physical exercise will deplete glycogen stores, which will typically not be fully replenished due to the low intake of carbohydrates.

Light endurance exercise (e.g., walking) is normally easier to maintain with a depleted “glycogen tank” than strength training, because light endurance exercise relies heavily on fat oxidation. It uses glycogen, but more slowly. Strength training, on the other hand, relies much more heavily on glycogen while it is being conducted (significant fat oxidation occurs after the exercise session), and is difficult to do effectively with a depleted “glycogen tank”.

Strength training practitioners often will feel fatigued, and will probably be unable to generate supercompensation, if their “glycogen tank” is constantly depleted. Still, compensatory adaptation can work its “magic” if one persists, and lead to long term adaptations that make athletes rely much more heavily on fat than the average person as a fuel for strength training and other types of anaerobic exercise. Some people seem to be naturally more likely to achieve this type of compensatory adaptation; others may never do so, no matter how hard they try.

Another implication is that you should not worry about short-term weight variations if your focus is on losing body fat. Losing stored water and glycogen may give you an illusion of body fat loss, but it will be only that – an illusion. You may recall this post, where body fat loss coupled with muscle gain led to some weight gain and yet to a much improved body composition. That is, the participants ended up leaner, even though they also weighed more.

The figure above also gives us some hints as to what happens with very low carbohydrate dieting (i.e., daily consumption of less than 20 grams of carbohydrates); at least at the beginning, before long term compensatory adaptation. This type of dieting mimics fasting as far as glycogen depletion is concerned, especially if protein intake is low, and has many positive short term health benefits. The depletion is not as quick as in a fast because a high fat and/or protein diet promotes higher rates of fat/protein oxidation and ketosis than fasting, which spare glycogen. (Yes, dietary fat spares glycogen. It also spares muscle tissue.) Still, the related loss of stored water is analogous to that of fasting, over a slightly longer period. The result is a marked weight loss at the beginning of the diet. This is an illusion as far as body fat loss is concerned.

Dietary protein cannot be used directly for glycogenesis; i.e., for replenishing glycogen stores. Dietary protein must first be used to generate glucose, through a process called gluconeogenesis. The glucose is then used for liver and muscle glycogenesis, among other things. This process is less efficient than glycogenesis based on carbohydrate sources (particularly carbohydrate sources that combine fructose and glucose), which is why for quite a few people (but not all) it is difficult to replenish glycogen stores and stimulate muscle growth on very low carbohydrate diets.

Glycogen depletion appears to be very healthy, but most of the empirical evidence seems to suggest that it is the depletion that creates a hormonal mix that is particularly health-promoting, not being permanently in the depleted state. In this sense, the extent of the glycogen depletion that is happening should be positively associated with the health benefits. And significant glycogen depletion can only happen if glycogen stores are at least half full to start with.

Tuesday, October 19, 2010

I am yet to be convinced that grilled meat is truly unhealthy in the absence of leaky gut problems. I am referring here to high heat cooking-induced Maillard reactions and the resulting advanced glycation endproducts (AGEs). If you are interested, see this post and the comments under it, where I looked into some references provided by an anonymous commenter. In short, I am more concerned about endogenous (i.e., inside the body) formation of AGEs than with exogenous (e.g., dietary) intake.

Still, the other day I had to improvise when cooking meat, and used a cooking method that is considered by many to be fairly healthy – slow-cooking at a low temperature. I seasoned a few pieces of beef tenderloin (filet mignon) for the grill, but it started raining, so I decided to slow-cook them in a frying pan with water and some olive oil. After about 1 hour of slow-cooking, and somewhat to my surprise, they tasted more delicious than grilled!

I have since been using this method more and more, with all types of cuts of meat. It is great for round steak and top sirloin, for example, as well as cuts that come with bone. The pieces of meat come off the bone very easily, are soft, and taste great. So does much of the marrow. You also end up with a delicious sauce. Almost any cut of beef end up very soft when slow-cooked, even cuts that would normally come out from a grill a bit hard. Below is a simple recipe, for round steak (a.k.a. eye round).

- Prepare some dry seasoning powder by mixing sea salt, black pepper, dried garlic bits, chili powder, and a small amount of cayenne pepper.- Season the round steak pieces at least 2 hours prior to placing them in the pan.- Add a bit of water and olive oil to one or more frying pans. Two frying pans may be needed, depending on their size and the amount of meat.- Place the round steak pieces in the frying pan, and add more water, almost to the point of covering them.- Cook on low fire covered for 2-3 hours.

Since you will be cooking with low fire, the water will probably not evaporate completely even after 3 h. Nevertheless it is a good idea to check it every 15-30 min to make sure that this is the case, because in dry weather the water may evaporate rather fast. The water around the cuts should slowly turn into a fatty and delicious sauce, which you can pour on the meat when serving, to add flavor. The photos below show seasoned round steak pieces in a frying pan before cooking, and some cooked pieces served with sweet potatoes, orange pieces and a nectarine.

A 100 g portion will have about 34 g of protein. (A 100 g portion is a bit less than 4 oz, cooked.) The amount of fat will depend on how trimmed the cuts are. Like most beef cuts, the fat will be primarily saturated and monounsatured (both very healthy), with approximately equal amounts of each. It will provide good amounts of the following vitamins and minerals: iron, niacin, phosphorus, potassium, zinc, selenium, vitamin B6, and vitamin B12.

Monday, October 18, 2010

Clive Parkinson will be sharing ideas from his new paper, A Brightly Coloured Bell-Jar, on Tuesday 2nd November at 5:00pm...he'd appreciate your feedback. Please email artsforhealth@mmu.ac.uk if you'd like to attend.

Monday, October 11, 2010

Blood glucose levels in birds are often 2-4 times higher than those in mammals of comparable size. Yet birds often live 3 times longer than mammals of comparable size. This is paradoxical. High glucose levels are generally associated with accelerated senescence, but birds seem to age much slower than mammals. Several explanations have been proposed for this, one of which is related to the formation of advanced glycation endproducts (AGEs).

Glycation is a process whereby sugar molecules “stick” to protein or fat molecules, impairing their function. Glycation leads to the formation of AGEs, which seem to be associated with a host of diseases, including diabetes, and to be implicated in accelerated aging (or “ageing”, with British spelling).

The graphs below, from Beuchat & Chong (1998), show the glucose levels (at rest and prior to feeding) and HbA1c levels (percentage of glycated hemoglobin) in birds and mammals. HbA1c is a measure of the degree of glycation of hemoglobin, a protein found in red blood cells. As such HbA1c (given in percentages) is a good indicator of the rate of AGE formation within an animal’s body.

The glucose levels are measured in mmol/l; they should be multiplied by 18 to obtain the respective measures in mg/dl. For example, the 18 mmol/l glucose level for the Anna’s (a hummingbird species) is equivalent to 324 mg/dl. Even at that high level, well above the level of a diabetic human, the Anna’s hummingbird species has an HbA1c of less than 5, which is lower than that for most insulin sensitive humans.

How can that be?

There are a few possible reasons. Birds seem to have evolved better mechanisms to control cell permeability to glucose, allowing glucose to enter cells very selectively. Birds also seem to have a higher turnover of cells where glycation and thus AGE formation results. The lifespan of red blood cells in birds, for example, is only 50 to 70 percent that of mammals.

But one of the most interesting mechanisms is vitamin C synthesis. Not only is vitamin C a powerful antioxidant, but it also has the ability to reversibly bind to proteins at the sites where glycation would occur. That is, vitamin C has the potential to significantly reduce glycation. The vast majority of birds and mammals can synthesize vitamin C. Humans are an exception. They have to get it from their diet.

This may be one of the many reasons why isolated human groups with traditional diets high in fruits and starchy tubers, which lead to temporary blood glucose elevations, tend to have good health. Fruits and starchy tubers in general are good sources of vitamin C.

He argues that we should be doing all we can to slow aging, not just waiting for it to happen. Chromium and other nutrients should be part of that.

Now, once again, we're discussing caloric restriction and the role of lowering fasting glucose levels. Glycation is involved with the aging process. You could say that "diabetes represents early aging."

The summary is that long-term dietary supplementation to ameliorate insulin resistance will increase a person's lifespan -- but no clinical trials because we can't live that long.

He discussed how to do a longevity study on rats: Zucker fatty rats, rats observed daily, model diets, groups receiving supplementation. He shows us the different formulas he's been using with chromium along with garlic, or garcinia cambogia, or maitake mushrooms.

He noted that sometimes when you add other stuff in formulas, it can change the whole outlook of the results.

"We think that everything in metabolic syndrome is caused by insulin resistance," he says. So, the level of chromium can be important because it can determine the level of glucose and insulin.

A specific amount of chromium can increase lifespan, but a little less cannot. Also, anti-diabetic drugs like metformin prolongs life, while other drugs shorten them.

It's important to keep glucose levels down, but not forget about the hyperinsulinemia. For longevity, you need to focus on both. When circulating insulin levels is lower, you live longer.

He ends with a cartoon on how we used to think the Russians lived longer because of yogurt, but later "to hell with yogurt." There are lots of questions, and he hopes that someone in the audience can one day answer them for him.

Q and A

What about vanadium?

He really backed off on vanadium because when fed to rats, they wouldn't eat and they lost weight.

What about spending time on insulin levels?

Preuss wants to do more studies on insulin levels to see about increasing lifespan.

Homocysteine, an sulfur amino acid, has been used over and over again marker for cardiovascular events. However, it is complicated so Jacob Selhub is going to talk about its particulars this morning at American College of Nutrition conference in New York City.

He starts by going through all the metabolic pathways that homocysteine is involved in, with methionine and SAM, as well as serving as a source for cysteine.

Hyperhomocysteinemia, he says, is caused by deficiencies in CBS, MTHFR, or in enzymes of B12 metabolism.

He tells the story about how back in 1969, pathologist McCully was studying how two children died of hyperhomocysteinemia. The pathology was identical, but causes were different.

The pathologies were arteriosclerosis. Even low levels of homocysteine was responsible for CVD. At the time, the idea was not accepted because the focus was on cholesterol.

Clinical trials? There have been a few, he says. In randomized controlled trials of folic acid supplementation, most showed lower homocysteine, but did not help cardiovascular disease (no benefit) (Miller et al Am J Card 2010).

He notes that hyperhomocysteinemia is related to other factors too. Being male is higher risk factor. It's very complicated, and he shows us more pathways again.

In the next decade, he says we need to look at the B vitamin pathways as a way to understand the disease.

NHANES research shows that vitamin D deficiency is associated with increased risk of frailty.

What about infectious disease? Elderly with higher serum 25-D levels don't get sick as often (Chesney, J Peds, 2010), so maybe vitamin D should accompany vaccinations.

She's now talking about how low vitamin D levels is associated with multiple sclerosis later in life, as well as rheumatoid arthritis and depression. In fact, vitamin D deficiency is associated with worse outcomes.

Lower vitamin D is also associated with higher risk of gum disease. Those with higher levels have less tooth loss.

What about cancer? Higher levels of vitamin D is related to a 50 percent reduction of breast cancer, reduced risk of colorectal cancer, and prostate cancer.

However, as a cautionary note, vitamin D in levels above 40ng is associated with higher risk of pancreatic cancer.

What about CVD? Living at higher latitudes increases risk of hypertension and cardiovascular disease. Vitamin D deficiency increases cardiovascular events by 62 percent.

Just this week, a study shoerd that patients with heart failure and low levels of vitamin D had a higher risk of all-cause mortality.

In general, low serum 25-D levels is associated wit increased risk of death, higher mortality rates, according to several studies and meta-analyses.

In summary, vitamin D is associated with several major chronic, age-related diseases and the elderly should consider supplementation. She recommends an intake of 1,000 IU a day with assessment of 25-D serum levels.

She also briefly talks about D3 versus D2 and why it should not matter which is used, since they both work (Holick JCEM 2008).

Do we age at different rates? At the American College of Nutrition conference today, we are being treated on this subject entitled "Nutritional and Hormonal Influences on Aging" by Nir Barzilai, MD, of Albert Einstein College of Medicine.

"Aging is the major risk factor for death from all chronic diseases," Dr. Barzilai says, so we should be focused on strategies to modulate aging.

Is lifespan determined by genes or the environment? This is not a really good question, he says. It's about "50 50" because it's really "genes in an environment." But even if it was 20 percent genetics, then you can still change the environment and increase lifespan.

He gives an example about how caloric restricted animals decreases all causes of death. In calorie-restricted animals fat is melted away, so this caused Barzilai to question, "what is the role of adipose tissue in aging."

In an experiment on Zucker diabetic fatty rats, those with visceral fat removed lived significantly longer. The visceral fat removal prevented diabetes in the rats, which clearly shows that visceral fat is biologically active and causes diabetes.

So, can a study design depict the challenges of genetics in aging? There is a major barrier, however, in conducting a study of centenarians. You don't have controls. As a control, you could use offspring of centenarians (Ashkenazi Jews).

Barzilia goes to a centenarian's home and always asks, "Why do you think you lived so long?" In one example, there was a whole set of siblings who were centenarians. He put some data together on what was found.

(He shows the data and compares it to NHANES and it appears similar. In fact, some smoked and overall they exercised less.

"If anything, this group was worse," said Barzalai. From age-related disease perspective, however, their age had been delayed for about 30 years.

Now, he says, we have an opportunity that no one else has because we can study specific genotypes and look at modeling changes in the frequency of a genotype as a function of age.

We can track the frequency trends of favorable longevity genotypes, which all have phenotypes. The best thing, obviously, is to have longevity running in the family. Plus, high HDL is a very good marker of a longevity genotype.

An interesting theory is the "rate of living" theory of aging that the more metabolically active you are, the shorter the life.

We've showed that a CETP-W genotype is protective. Merck is also developing a CETP inhibitor, which he is anxiously awaiting.

Dr. Barzilai is now showing images of several centenarians, who are so very cute, and some of the interactions they have.

In summary, the fact is that we all have different rates of aging and that both genetics and environment play factors, but it can be different for each of us.

Friday, October 8, 2010

Beth Dixon, Ph.D., from the Department of Nutrition of New York University is going to try to talk about Dietary Guidelines for Americans (but it sounds like she's got a sore throat).

Out of the 2005 Dietary Guidelines for Americans, she says, came a focus on consuming a variety of foods, controlling calorie intake, increasing fruits and vegetables, etc. We know all this, but what was new was the USDA Food Guide (based on MyPyramid) and the DASH eating plan.

The USDA Food Guide were designed to be flexible with 12 different plans at a 2000-calorie level with main food groups (like fruits, vegetables) given in amounts (like 2 cups per day). There are also subgroup categories such as vegetables having a subgroup of dark green vegetables, orange vegetables, etc.

"The idea behind these food plans is to focus on nutrient-dense foods," she says. "There's a behind-the-scenes way of counting food groups."

To get to the concept of diet quality, the USDA folks developed a Healthy Eating Index. It's based on the idea that there is some way to measure diet quality that assesses adherence to a diet plan. Again, like other indices, it has weighted scoring of various foods.

There have also been recent revisions to the HEI such as "SoFAAS" (which we'll keep hearing about) that represents solid fats, alcohol and added sugars.

She goes on with a highlight of Guenther et al. data in Nutrition Insight on NHANES showing that there is a significantly lower intake of whole fruits and whole grains, higher dairy (mostly cheese).

And she also looks at Krebs-Smith et al (J Ntr 2010) data showing that many Americans do not meet dietary recommendations.

More studies... (my wrists hurt)

There are lots of total diet indices that show that a better quality diet is associated with better markers in cardiovascular disease.

Stay tuned for 2010 Dietary Guidelines for Americans with updates to the HEI. A direct quote from the new guide, "Recommended intake amounts in the USDA Food pattern remains unchanged from 2005 with the exception of the vegetable subgroups [red orange veg and cooked dry beans and peas]."

She's closing now... whew! ... with Reedy et al data from 2010 Am J Prev med on The Food Environment. Looks like it's in a typical American environment you can potentially find it easy to eat whole grains, but harder in other areas like fruits and vegetables.

Greek, Italian or Spanish? What kind of Mediterranean-style diet are we talking about when we consider eating a Mediterranean diet? Talking about this right now at American College of Nutrition conference in New York City is Paul Jacques, S.c.D., FACN.

Well, mostly it's Greek, he says, which recommends eight servings of whole grains, six servings of vegetables, three servings of fruits, two servings of dairy, one and a half servings of wine, exclusive use of olive oil, fish, and little meat.

Many of the studies are based on the Greek Mediterranean-style diet.

So, Jacques captured the most frequently consumed foods based on NHANEs in the U.S. and tried to find how a Mediterranean diet could be followed in using 1,250 commonly consumed U.S. foods.

However, there are studies that are on anything but the Mediterranean diet. He cites an example of a cohort study on Mediterranean dietary pattern and mortality among young women in Sweden. They found that young women who adhered closely to a traditional Mediterranean diet had reduced risk of mortality.

He's skeptical because "I find it hard to believe that there are really this many young women eating a Mediterranean diet" next to Baltic Sea.

There are also French studies that compared a traditional Mediterranean diet and a standard American Heart Association diet that found no difference in clinical outcomes.

As a summary, he presents a table of intervention studies of Med diet and adiposity that were six months or longer (several countries: Spain, Germany, Italy, U.S.). You can see that some type of diet intervention significantly lowers BMI.

But "a diet is only good if people can adhere to it," he says. So, he highlights one particular diet where it showed that people adhered more often to a Med diet than a low-fat diet.

Then, he shows the data of the famous Shi et al. DIRECT study from NEJM where it shows that people find it easier to adhere to a Med diet versus a low-carb or low-fat diet.

As far as observational studies, you must ask "Are the studies really on the Mediterranean diet?"

The ones that are percentile-based diet scores: Many are not based on specific recommendations, but arbitrary, population-specific values for assigning adherence and are not appropriate for use in non-Mediterranean countries.

A Mediterranean-style Diet Pattern Score (MSDS) is criterion-based score using recommendation from a Med diet pyramid, continuously scaled without arbitrary cut-off points, accounts for over-consumption of foods, and adjust for proportion of energy from non-Med-style foods.

"For example, where do French fries fall in the Mediterranean pyramid?" he says. The scoring is based on weighted scores with points per serving and penalizations. He shows us some equations he uses about how to develop the MSDPS scores.

He keeps reminding us that "no one really in the U.S. consumes the Mediterranean diet." So, he says, we have to be careful in saying that "greater adherence to a Med diet is associated with this or that." We have to be concerned about what exactly those patterns are; they may have a few more components to the Med diet, but not consuming a total Med diet.

It would be better to explain that people consuming a "partial Mediterranean diet" or whose diets "had more components of a Mediterranean diets" have improved metabolic traits. If you left it to Jacques, all the studies would be more specific in pointing out those components.

He goes on with other studies that show that "basically, adherence to Mediterranean diet based on commonly consumed foods in American's diets would largely address short-fall nutrients."

Few studies, particularly those in non-Mediterranean countries are not really the right diets. In spite of limitations, larger intervention studies demonstrate health benefits. And, again, more research is needed. Etc, etc.

Speaking on HPLC diets for obesity is Mount Sinai School's Jeffrey Mechanick, M.D., who starts out with the theoretical advantage and perspective of low-carb diets.

There is a clinical problem of obesity, type-2 diabetes and cardiovascular disease. And there is controversy about whether or not total calories matter or if there is something to the composition of calories as in a high-fat, high-protein, low carb diet.

Dr. Mechanick has an interest in Paleo dieting since it is based on genomic programming and evolutionary biology. Like McKeown before him, he says that Mediterranean diet is no single diet, but is characterized by a diet high in fruits and vegetables, moderate fish and alcohol, high in olive oil, high in polyphenols and little meat. The cardiovascular benefits have been demonstrated.

But there are concerns there's evidence for lack of long-term benefit, increased risk for kidney stones, ketosis and bad breath, low in fiber, calcium, magnesium, potassium, iron, folate, thiamine; is higher in saturated fat then increase in CVD risk, increase cancer risk if low in fruits and vegetables.

What's the compromise? To tailor a HPLC where carbohydrate is replaced with healthy fats like MUFAs, PUFAS and omega-3s along with high biological value proteins, especially plant proteins, low-glycemic complex carbs.

Dr. Mechanick then goes into quite a few of the studies regarding low-carb diets and comparisons to other diets. I'm going to try to summarize by saying that: According to studies and meta-analyses on RCTs, a Mediterranean-style low-carb diet leads to same weight loss and is healthier than other low-carb diets.

However, Dr. Mechanick notes, the data do not support that all people should be on low-carb diets.

He concludes that there are inconclusive results of HPLC diets based on well-conducted PRCTs, there are inconsistencies due to problems with surrogate markers, and that we need a systems approach to better understand complexities.

Next up at American College of Nutrition conference, we're about to enjoy a talk given on "Nutrition and Chronic Disease: Advantages of a Diet Pattern and Health Outcomes" given by Nicola M. McKeown, Ph.D., of the USDA Human Nutrition Research Center on Aging at Tufts University.

"Trying to measure dietary exposures is very difficult," sayd McKeown. The nature of nutrition is extremely complex, and she quotes Walter Willet on the complexity (which makes me like her already). "A single nutrient may be confounded by an overall dietary pattern."

Single-nutrient approaches ignore complexity of diets, biological interactions, and there is difficulty to detect small effects and observe health effects of single components.

How do we research with this complexity? We may be interested in a dietary pattern, a food group, an individual food, single nutrients, and bioactives (a top-down approach).

Why study dietary patterns? They represent the interactions and cumulative effects of dietary components on disease risk. They capture potential foods and nutrient synergy. They help generate hypotheses about biological mechanisms, and they can translate to dietary pattern recommendations.

In epidemiology, there are two ways to derive dietary pattern approaches are theoretical (hypothesis-oriented) and empirical (exploratory-oriented). "The data drives the patterns," she says. Most of the time it's based on food frequency questionnaires. The input variables may be frequency, weight, daily percent of energy contribution.

With a factor analysis, the goal is to identify common factors that explain variance in the dietary data. it's based on correlation/covariance matrix of the food groups. It aggregates specific food groups on the basis of degree of use.

She then shows examples where various food groups are weighted based on factor loading of top contributing foods. A Western dietary pattern, for example, is higher in meat, processed meat, and butter in comparison to a prudent dietary pattern.

Cluster analysis (which you may "hear a lot about in the literature") is based on aggregates of individuals into distinct food groups. It's sensitive to extreme outliers so treatment of input variables is important.

She gives a few examples of cluster analysis, such as:

Cluster 1: reduced-fat dairy, fruits, and whole-grains.

Cluster 2: refined grains and sweets.

Cluster 3: Beer (lots of men were in this category).

Cluster 4: Soda (people in this category were found to have higher fasting insulin)

From a research standpoint, there have been a few diets with great interest including the Mediterranean diet and low-carb diet. There have been indexes developed for these two diets as well as the Healthy Eating Index.

The indexes can be used to create a "diet score," each of which are based on cut-points of various food groups with criteria that determine weight of each food that contribute to the score. [The diet scores look like a handy tool for helping people stay on track.]

The 2005 Dietary Guidelines for Americans Adherence Index (DGAI) are based on food intake recommendations and it penalizes for overconsumption of discretionary energy and energy-dense foods (chips and French fries). They also had a "variety score" when people had various foods in the diet.

When individuals adhere to the DGAI, they had a lower prevalence of metabolic syndrome. Based on the scoring approach, McKeown says, it's possible for people to get the same score and have different dietary patterns.

Regarding the Mediterranean dietary pattern, McKeown reminds us that "there is no single Mediterranean diet," but it's based on patterns, so a diet score can be useful for adhering to the dietary pattern.

When discussing low-carb dietary patterns, they have similar macronutrient composition, but may have different dietary quality. There should be scores indicated depending on the choices of fat -- animal or vegetable. She is careful to note that it's important to consider that when you talk about macronutrients to consider substitutions for foods eliminated.

She closes by saying that there is subjectivity in defining cut points in indices. Indices may be a good index of diet quality but not of disease risk. High scores are rare, but average scores can be achieved a number of different ways. Eating patterns associate with other health behaviors.

As part of Symposium II at American College of Nutrition conference in New York City, we are now enjoying a talk by PATH Medical director Eric Braverman, M.D., FACN.

Braverman starts out talking about how "the brain is the most important organ" and you can have "too highs and too lows" such as in blood pressure, etc. He says he operates on the view that the purpose of being a doctor is to improve health in dramatic ways, which he adds should be measured.

He has a slide up of several examples of aging patterns: "pause," "decline in," and "onset age." One example is "osteopause," "bone sensity" and "30", or "menopause," "estrogen, progesterone, and testosterone in women" and "40."

Brain aging, from his perspective, has to be simplified to get anywhere. He "boils down" to loss of neurotransmitters and hormones in aging that leads to widespread down.

"Aging is marked by neuropsychatric decline," he says, along with other factors involving neurotransmitters and hormone loss.

Braverman is going to focus on leptin now. First thing to not forget is that it's both an adipose hormone and a hypotholamic hormone. It's an integral component of energy homeostasis and body weight regulation.

There's a close interaction also with leptin and dopamine D2 receptors, as well as other genes involved that are associated with high BMI.

"Leptins are kind of funny because when they go low they're associated with dementia in aging," he says. "Ironically, on the other side, high leptins in obesity are correlated with decreased testosterone, estrogen as well."

Leptin impinges on many brain areas in addition to the hypothalamus. If you have a sick body, you have a sick brain.

But let's talk about obesity, he says, it's what kills you, speeds up the aging process and reduces lifespan by 15 years. One of five brain problems costing the country at least a hundred billion or more is obesity, addiction, neuropsychiatric problems, violence and cognitive impairments.

There should be more awareness between the distinction of Normal-Weight Obesity and Overweight-Obesity.

"I really see muscle mass as critical," he says. "If you're thin and flabby," all the bad things that come with obesity are coming for you any way including metabolic syndrome (increased triglycerides, increased LDL, lower HDL, etc.).

He likes the DEXA scan much better than BMI. In fact, he had a few slides on this topic. But that's a different story. In summary, he says, "the obesity epidemic is much worse than we think."

Aging is marked by "metabolic imbalances," then shares a little poem which he calls the "Description of Aging."

He's going to summarize that obesity epidemic speeds up aging, leptins play a role (it's the "connection between the brain and fat cells"), and there's a synergistic effect dopamine, acetylcholine, GABA and serotonin that is the "Brain and Body Connection."

We can emphasize brain and body repair mechanisms with the "four horesemen": Natural, pharmaceutical, hormonal and lifestyle agents to promote the synergistic action of dopamine, acetylcholine, GABA and serotonin.

He's got a whole table with several agents. I see caffeine on there, which is what I think I need, plus fish oil, acetyl carnitine, CoQ, theanine, tryptophan, magnesium, folic acid, etc.

"If we're going to keep our intelligence with age, we're gonna have to have neurogenesis," he says. "I was taught that there was one neurotransmitter in one neuron. Now we know that there are 70 neurotransmitters in a neuron."

---

For such an interesting title, not sure this talk delivered. I guess I was hoping for a step-by-step on how to prevent and reverse brain aging. But, diet and exercise, eating lots of natural agents and pharmaceuticals seems to be the key.

Now, for the second keynote at American College of Nutrition conference in New York City we're listening to Mark Mattson, Ph.D. He starts out talking about his work in the laboratory of neurosciences at National Institutes of Aging.

He talks about what happens during aging in the brain.

More and more as people get older, neurons age and die, predisposing us to Alzheimer's and other brain diseases. The mechanisms on how this happens are being shown and he discusses the different pathways.

Current trends in Alzheimer's showing it's a huge issue that's not being dealt with. We need a war on it like we have on cancer. Many people die from Alzheimer's and it's a tax on society.

He discusses amyloid plaques and neurofibrillary tangles (with tau) that is involved in AD pathogenesis.

There's a number of animal models for AD such as transgenic mice with overexpression of mutated amyloid-precursor protein. Also, PS1 mice.

Mattson manipulates diets of AD-prone mice to see how diet affects their cognitive function, memory, and amelioration of AD behavior.

Intermittent fasting and calorie restriction ameliorated AD behavior changes. He thinks that neurons can be stimulated by these diets to protect themselves against the amyloid protein. He shows us data on how CR reduced tau levels, but IF did not.

They also used "couch potato mice" model of AD: overfed, sedentary. Of course, these are great controls.

They wanted to show an effect in primates, so performed a study in rhesus monkeys. They took the monkeys and reduced their calories by 30 percent for 11 months. They tested their motor function, dopamine. They injected a toxin called MPTP.

Both the animals on the normal diet and CR diet had deficits in motor function, but CR had less seeming to have a protective effect from a functional endpoint. When measured for dopamine, there was major depletion in the striatum in both. When measured for BDNF, the CR had higher levels of BDNF.

In a stroke model, they took young, middle-aged, or old mice on either IF or normal diets. They then damaged the cerebral cortex and measured neurological deficit. There was significant benefit for the young and middle-aged mice on IF, but not in old.

"So start early," he says. Exercise, eat less when you're younger to prevent Alzheimer's in the future. IF reduced inflammation in the young and middle-aged, but not in old.

Mattson starts talking about type 2 diabetes now. The world prevalence of diabetes is rising. This disease leads to problems later on in the brain, as shown in more mice models (like leptin-receptor mutant mice), which he summarizes.

- reduced BDNF levels- l wer neurogenesis

Diabetes reduces neurogenesis, but what about interactions with exercise or calorie restriction? Both exercise and CR increase BDNF levels.

Some drugs work by involving BDNF. There are also several fruits and vegetables, but he doesn't think they have an intrinsic factor as antioxidants. Instead, he said, they have toxins concentrated in the skin meant to repel insects. Lots of these plants have natural pesticides, so Mattson acquired many of these natural chemicals to see which produce resistance to neurogenerative disorders.

OK, back to talking about IF, this time about a study showing that IF improves cardiovascular risk factors under stress in animals.

-The body temperature is up on the feeding day, down low on the fasting day. -Heart rate variability was measured too. Higher heart rate variability is a good thing, because it shows adaptability. IF improved heart rate variability.-Higher levels of BDNF

Interesting thing, he notes, when they infused BDNF in mice, they showed better heart rate variability.

Human studies? Mattson talks of Jim Johnson's work on subjects with moderate asthma on alternate-day calorie restriction. The subjects adapted to the diet, lost bodyweight, their mood increased, but importantly their asthma improved.

He intends to conduct a 3-year double-blind, randomized trial on a drug (Exendin-4) to treat Alzheimer's disease, by testing CSF biomarkers. He is optimistic and says at least he knows the drug should help with blood glucose management.

---

Unfortunately, Mattson ran out of time, but the presentation was awesome! Good to know we have serious scientists like this working on AD.

Surprisingly, with all the talk about CR, IF and Alzheimer's, not a word was said about Sirtuin 1 activation, so I asked Dr. Mattson his opinion on the research, specifically Guarente's paper showing that SIRT1 activation inhibited two pathways in the progression of AD.

Mattson responded with a dose of skepticism about sirtuins and their potential, at least as a treatment in the diseased state when they'd use up a lot of NADPH at a time when the brain needs it.

Our keynote presentation at American College of Nutrition conference in New York City was neurologist David Perlmutter, MD. He started off talking to us about the "uniqueness of the human brain."

However, inflammation and oxidative stress ultimately lead to neurological degenerative disease. The brain's antioxidant defenses are limited and inflammation happens in the brain just as anywhere else.

He showed us MRIs of classic brains and those of Alzheimer's patients (along with activated microglia). "This is the picture of what is happening. It is the brain on fire."

In Parkinson's there is an increased density of glial cells expressing inflammatory cytokines, showing oxidative stress and inflammations is related to the disease too.

Typically when Perlmutter helps Parkinson's patients, he tells them the drugs don't treat the disease only the symptoms. "You need to treat the fire," he says.

Now, we also can "unlock the potential of our genes," he says. "It's a fascinating time. We call the study epigenetics and we're learning that we can modulate gene expression."

This is why he is so interested in nutrition: epigenetics. We can modify how our genes express, such as the Nrf2 activation to deal with inflammation and free radical formation.

Activation of transcription factor Nrf2 is powerful, says Perlmutter. It's the "guardian of redox homeostasis," he notes referencing a study.

He says we're going to learn a lot about Nrf2 (along with other factors in epigenetics) in the future, so also finding potential targets for lowering oxidative stress.

"If you're training for a marathon or not sleeping well, these are the pathways that helped protect us. When we were hunter-gatherers and didn't have enough calories, these are the pathways that allowed us to pass on our genes."

He then began talking about curcumin's actions on reducing oxidative stress and protecting the hippocampus in mice, which is key for the protection of the brain against Alzheimer's.

"Curcumin is not only able to lower oxidative stress, but reduce plaque burden [by 43-50%]."

More brain scans were shown, this time of amyloid burden, from a study, and he went back to show that the Indian spice shows "promise for the prevention" of Alzheimer's (Lim et al. J Neuroscience).

One of the principal activators of Nrf2 is sulforophane (from broccoli, for example) which is why we always use this as a good detoxifier. He shows an animation about how broccoli creates the activation of Nrf2.

Coffee also is very good for activating the pathway, which is why he showed us an animation of a businessman worshipping coffee (great for oxidative stress).

"Early events in the pathogenesis of Alzheimer's is oxidative stress," he says, so we need to focus on prevention with antioxidants and upregulating antioxidant defense mechanisms.

If you are worried about Alzheimer's because of family history or oxidative stress, then you should consider nutrition to prevent. He says we should also be measuring for oxidative stress early on, especially in Alzheimer's, and be sure people are getting the basics like vitamins A and C.

So many of our diseases seem to be related to toxins too, like Parkinson's (and he shows us an article about pesticides being linked to Parkinson's).

Perlmutter then went on to discuss Brain-Derived Neurotrophic Factor, a neurotropin crucial for integrity of adult neurons and for neurogenesis.

Caloric restriction, exercise, etc., stimulate neurogenesis -- increasing number of neurons -- and he references a study that was the first evidence that diet could influence neurogenesis.

He shows scans of brains on diet restriction where new cells are being formed, which fully differentiate into neurons. What are the factors that can enhance stem-cell therapy in your brain? Calorie restriction.

In humans, there is an upregulation in BNDF with only 25 percent reduction in calories, and diet is a powerful epigenetic factor that could avoid degeneration of the brain into Parkinson's or Alzheimer's.

When we restrict calories, we see produced ketones, reduction of free radicals, and turns on mitochondrial replication. This happens by activation of uncoupling protein so there's less free ATP, less radicals, increased mitochondrial replication, then an increase of ATP and energy.

He shows us images of a mitochondrion and says it's actually involved in controlling DNA (with its own "feminine" DNA). The mitochondria also are involved in whether or not cells live or die.

As a society what are we doing to help people avoid Alzheimer's, which is a devastating disease, and where many of us are at risk.

He puts up a slide that says "upavasa" (some kind of old word about ancient knowledge of brains), then goes back to the modern science. We've come a long way. He shows us pathways again to hone in on the message that by activating specific pathways (through a ketogenic diet) for preventing Alzheimer's.

A ketogenic diet upregulates mitochondrial biogenesis, and so does physical exercise, which augments production of neurogenesis. Exercise also extends the length of dendrites, important in neuroplasticity.

He shows slides on exercise where mice had "dramatic" enhancements in proliferation of neural stem cells.

Then, he talks about how exercise improves mental function in adults at risk for dementia. It's so important.

"Everyone is at risk," he says, since we may have each had our own experiences that put us at risk for dementia.

"If you could create a drug that could do this (enhance cognitive function), it would be the biggest-selling drug of the day," he says, noting that exercise is free for us all to take advantage of now for the plasticity of our brains.

Scientists (Frontiers in Neuroscience, Aug 2010) found that walking increases functional connectivity in the aging brain and attenuating age-related brain disfunction. Physical exercise is a key that is better than any pharmaceutical drug for enhancing Nrf2.

We also know, he says, that eating fish helps people avoid brain degeneration, since DHA normalizes Nrf2. The relative risk of Alzheimer's is reduced by around 70 percent in those that have diets high in DHA (Morris et al, 2003, Arch Neurol).

"If you're going to jump out of an airplane, then you want a wear a parachute," he says. And he tells us we shouldn't completely rely on randomized, controlled trials.

Perlmutter wrote an article previously called "Making New Connections" where he discusses learning about how the brain was able to change, despite prior thinking in medicine.

"New networks are being formed," he says. "The brain is remarkably plastic. It can repair itself." And through these pathways (Nrf2) we can enhance this effect of neurogenesis, neuroplasticity.

And he discusses Dr. Merzenich's (author of "Train your mind, Change your Brain") work showing how just mental activity can change the brain.

Plus, Andrew Newberg's work how meditation changes the brain in ways shown on brain scans, which he shows.

Perlmutter studied the anterior cingulate, which allows us to be empathetic, compassionate, socially aware, and intuition. It's strengthened by "spirituality" or any meditative state in which you feel comfortable.

He now discusses our prefrontal cortex and tells us many of us function on a more "primitive level" like fight-or-flight, from the amygdala (the reptilian brain) without thinking things through and becoming much more sympathetic, from the anterior cingulate (empathetic brain).

When we read the newspaper and feel the fight-or-flight, we often think from an "amygdala level." But we can favor the anterior cingulate through meditation, and by engaging in physical exercise, calorie restriction, eating DHA for enhancing Nrf2.

He talks about fasting now: fasting at ramadan, Jesus fasting, other fasting traditions. Fasting is a way to gain access to a higher brain.

He closes with quotes from Einstein, etc, about how through fasting, diet restriction, nutrition, we can become the "beings that we want to become."

After the talk, Dr. Perlmutter received a humanitarian award on behalf of ACN for his work in "Hope for Haiti."

Thursday, October 7, 2010

What are we doing about our national addiction to sodium? To present on this topic, we have Sonia Angell, MD, from the National Salt Reduction Initiative at the American College of Nutrition Conference in New York City.

"The most recently daily recommendation of 2,300 milligrams of sodium or lower is not being followed," says Dr Angell. So, who's to think that people will follow new recommendations of intake of no more than 1,500 milligrams?

How much is it about individual choice? Clearly, sodium intake is much higher in the U.S. than recommended, she says. What can industry do?

Many clinicians spend enormous amounts of time supporting high-risk populations, but what can be done about the overall population?

She asks, "How do we support choices?" Then she shows an example of two billboard signs placed next to each other, ironically: one advertising blood pressure readings, one advertising fast food.

Lewington et al showed that there is a linear increase of hypertension and cardiovascular disease. And the DASH study (Sacks, NEJM. 2001) shows clearly that by reducing sodium intake, we can make an impact on blood pressure.

One single intervention, salt reduction, says Angell, can save more lives than reducing smoking, statin therapy, and weight loss.

Where does salt come from? About 77 percent comes from processed and restaurant foods, which explains why it becomes so difficult for people to reduce it in their diets.

Even if one reduces caloric intake, people still end up with too much sodium because of the density of sodium in foods at home and when eating out.

"Sodium reduction initiatives are not new," says Angell, noting that scientists have been trying regulate salt intake since 1983.

The UK Salt Campaign had the goal of reducing salt intake by one third from 2005 to 2010 with gradual reductions throughout the food industry. The U.S. strategy is based on the UK successes with targeted goals of reductions in sodium in processed foods.

Decreasing sodium in foods by 25 percent over five years will reduce total sodium intake in population by 20 percent.

The National Salt Reduction Intake initiative includes creation of packaged and restaurant food databases, more than 100 meetings with industry, and targeted achievements.

They just finished a baseline evaluation in populations of New York City and will report again in 2014.

The message that Angell is delivering is that reducing sodium in foods doesn't mean that processed food will not sell as well. She then showed us a broad list of all the categories of foods where sodium is used. By setting targets on different products where reducing sodium is most feasible, industry can "shift the curve" of the food supply so that products overall consumed contain less sodium.

For example, they created 25 restaurant food categories. They analyzed for top 50 quick-service restaurants selling common items such as hamburgers, chicken sandwiches, etc. They set targets for key food categories to reduce sodium by amounts feasible by certain dates.

On April 26th, NSRI announced first company commitments including Unilever, Boar's Head, Kraft, Heinz, Starbucks, Subway, LiDestri, and Mars. They also got very good press. Angell praised these companies for showing leadership in improving the health of their customers.

Then, Angell began to explain next steps of NSRI to continue collaborations with national health organizations and the opportunities of having a strong, national database with mandated industry-reported nutrition information.

She says the NSRI has a planned announcement this fall of more collaboration with chief food companies.

To conclude, she says that national sodium reduction is crucial, that reduction initiatives are happening, and that collection of data (e.g. urinalysis) is feasible.

Industry Response

In the Q and A section there were plenty of questions about how industry responded to NSRI.

It has been a challenge for some companies, Angell notes (specifically companies like Burger King and McDonald's), so more education is necessary to increase the pressure on certain companies.

There was also a question of just how important salt intake would be on the population, since some people have no problems with sodium intake. Do we need more randomized, controlled trials.

Angel handled these questions very well, stating that "if reducing sodium in food doesn't make a difference in flavor, then no one really loses" and there is great evidence showing that the "majority of the population" will benefit.

She also answered my question about whether or not there were any salt substitutes that stood out to her as possible opportunities in the future. She answered that unlike with artificial sweeteners, there has been little development of artificial salt substitutes.

However, she adds that food manufacturers are beginning to discover ingenious ways of using salt crystals to give the impression of saltiness without over-concentrating the amount of sodium in processed foods.

When I asked about what reducing iodizdd salt intake would do to levels of iodine in the population, she cleared up some confusion: the message should not be to discontinue use of normal amounts of table salt, which supplies important iodine.

The mesage of NSRI is to reduce amount of sodium in processed foods ("processed foods don't use iodized salt") to reduce overall sodium intake in the diet.

Tuesday, October 5, 2010

The idea that calorie restriction extends human life comes largely from studies of other species. The most relevant of those studies have been conducted with primates, where it has been shown that primates that eat a restricted calorie diet live longer and healthier lives than those that are allowed to eat as much as they want.

There are two main problems with many of the animal studies of calorie restriction. One is that, as natural lifespan decreases, it becomes progressively easier to experimentally obtain major relative lifespan extensions. (That is, it seems much easier to double the lifespan of an organism whose natural lifespan is one day than an organism whose natural lifespan is 80 years.) The second, and main problem in my mind, is that the studies often compare obese with lean animals.

Obesity clearly reduces lifespan in humans, but that is a different claim than the one that calorie restriction increases lifespan. It has often been claimed that Asian countries and regions where calorie intake is reduced display increased lifespan. And this may well be true, but the question remains as to whether this is due to calorie restriction increasing lifespan, or because the rates of obesity are much lower in countries and regions where calorie intake is reduced.

So, what can the China Study II data tell us about the hypothesis that calorie restriction increases longevity?

As it turns out, we can conduct a preliminary test of this hypothesis based on a key assumption. Let us say we compared two populations (e.g., counties in China), based on the following ratio: number of deaths at or after age 70 divided by number deaths before age 70. Let us call this the “ratio of longevity” of a population, or RLONGEV. The assumption is that the population with the highest RLONGEV would be the population with the highest longevity of the two. The reason is that, as longevity goes up, one would expect to see a shift in death patterns, with progressively more people dying old and fewer people dying young.

The 1989 China Study II dataset has two variables that we can use to estimate RLONGEV. They are coded as M005 and M006, and refer to the mortality rates from 35 to 69 and 70 to 79 years of age, respectively. Unfortunately there is no variable for mortality after 79 years of age, which limits the scope of our results somewhat. (This does not totally invalidate the results because we are using a ratio as our measure of longevity, not the absolute number of deaths from 70 to 79 years of age.) Take a look at these two previous China Study II posts (here, and here) for other notes, most of which apply here as well. The notes are at the end of the posts.

All of the results reported here are from analyses conducted using WarpPLS. Below is a model with coefficients of association; it is a simple model, since the hypothesis that we are testing is also simple. (Click on it to enlarge. Use the "CRTL" and "+" keys to zoom in, and CRTL" and "-" to zoom out.) The arrows explore associations between variables, which are shown within ovals. The meaning of each variable is the following: TKCAL = total calorie intake per day; RLONGEV = ratio of longevity; SexM1F2 = sex, with 1 assigned to males and 2 to females.

As one would expect, being female is associated with increased longevity, but the association is just shy of being statistically significant in this dataset (beta=0.14; P=0.07). The association between total calorie intake and longevity is trivial, and statistically indistinguishable from zero (beta=-0.04; P=0.39). Moreover, even though this very weak association is overall negative (or inverse), the sign of the association here does not fully reflect the shape of the association. The shape is that of an inverted J-curve; a.k.a. U-curve. When we split the data into total calorie intake terciles we get a better picture:

The second tercile, which refers to a total daily calorie intake of 2193 to 2844 calories, is the one associated with the highest longevity. The first tercile (with the lowest range of calories) is associated with a higher longevity than the third tercile (with the highest range of calories). These results need to be viewed in context. The average weight in this dataset was about 116 lbs. A conservative estimate of the number of calories needed to maintain this weight without any physical activity would be about 1740. Add about 700 calories to that, for a reasonable and healthy level of physical activity, and you get 2440 calories needed daily for weight maintenance. That is right in the middle of the second tercile.

In simple terms, the China Study II data seems to suggest that those who eat well, but not too much, live the longest. Those who eat little have slightly lower longevity. Those who eat too much seem to have the lowest longevity, perhaps because of the negative effects of excessive body fat.

Because these trends are all very weak from a statistical standpoint, we have to take them with caution. What we can say with more confidence is that the China Study II data does not seem to support the hypothesis that calorie restriction increases longevity.

- The path coefficients (indicated as beta coefficients) reflect the strength of the relationships; they are a bit like standard univariate (or Pearson) correlation coefficients, except that they take into consideration multivariate relationships (they control for competing effects on each variable). Whenever nonlinear relationships were modeled, the path coefficients were automatically corrected by the software to account for nonlinearity.

- Only two data points per county were used (for males and females). This increased the sample size of the dataset without artificially reducing variance, which is desirable since the dataset is relatively small (each county, not individual, is a separate data point is this dataset). This also allowed for the test of commonsense assumptions (e.g., the protective effects of being female), which is always a good idea in a multivariate analyses because violation of commonsense assumptions may suggest data collection or analysis error. On the other hand, it required the inclusion of a sex variable as a control variable in the analysis, which is no big deal.

- Mortality from schistosomiasis infection (MSCHIST) does not confound the results presented here. Only counties where no deaths from schistosomiasis infection were reported have been included in this analysis. The reason for this is that mortality from schistosomiasis infection can severely distort the results in the age ranges considered here. On the other hand, removal of counties with deaths from schistosomiasis infection reduced the sample size, and thus decreased the statistical power of the analysis.

"All of these don't work 100 percent of the time, but every once in a while you see miracles happen," says Simon.

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I think the last quote summed it up. Great stories, but it doesn't do much for proving nutritional therapies help autistic kids. I would've liked to see more actual scientific research at this workshop.

Now we're going into Part 2 of the Autism and Nutrition Workshop at University of Bridgeport, with Gerri Brewster opening up with a lecture on the Dietary Interventions for Autistic Spectrum Disorders.

She begins with a discussion of current diets, which she says are designed to "facilitate healing" the GI tract to improve autism-linked symptoms like cognitive performance.

Clean diets should be the goal for everyone since according to California Department of Public Health showed that a "High rate of autism [is] seen in children exposed prenatally to organochlorine pesticides."

You have six times more incidence of autism in children from women who lived within 500 meters of fields with organochlorines (reference: www.cdph.ca.gov/prgramservices/news/documents/PH07-13%20Autism%20Study.pdf).

She goes on to suggest buying organic foods, avoiding the EWG "dirty dozen" and "stopping the deluge" coming into the bodies of these little ones.

Wow, she also has a thing against GM foods citing American Academy of Environmental Medicine's call for an immediate moratorium against GMOs in food.

The AAEM concluded, "There is more than a causal association between GM foods and adverse health effects."

Feingold diet is based on reducing phenols and salicylates in the diet. According to www.feingold.com, a little more than half of patients see improvement.

But the diet is pretty restrictive of many fruits and vegetables, nuts, etc.

The GFCF diet is based partially on the "Opioid Peptide Theory," which gathers that small proteins of 4-5 amino acids are identified as gluteomorohins and casomorphins, which are believed to get to the brain and cause an opioid effect.

But this theory was discredited since peptides resolved when the gut healed, so maybe only a marker of intestinal permeability?

Yet, surveys show that parents report that GF or CF causes improvement in almost half of patients. The parents reported that GFCF improves symptoms in 65 percent of patients.

Maybe eliminating GFCF (large proteins) reduces "total load on the gut" that allows for reduction of toxins getting into blood? This is the question Brewster has on her slide.

But GFCF has limitations, says Brewster. "You don't want to move into a lot of gluten-free junk food." Parents should focus on whole foods, limits on carb-laden foods.

It's also not usually enough to heal the gut, she says, so recovery is limited.

She says it's hard for parents to keep their kids on the GFCF diet. They say, "oh, it didn't work." But when Brewster asks them how long they stayed on it, they say, "two weeks."

The Specific Carbohydrate Diet was developed by Dr. Sydney Valentine Haas, which is an almost sugar-free and grain-free diet to heal the gut for people with gut problems ranging from Celiac to Crohn's disease.

"If they haven't done anything yet, then I don't get them started on anything else." They need to start with the basics first.

Simon's advice:

Many of the children are picky eaters, which may be due to a mineral deficiency like zinc.

You can sometimes see if they have yeast overgrowth by checking for white spots on their tongues.

Get a food sensitivity test -- keep in mind that there are times when a child will test and come back with no food allergies, but what they don't understand is that they can still be "sensitive" (to lactose, gluten, etc.).

What Brewster sees every day are children with gut issues, asthma, and food allergies, along with parents who have stories related to vaccine trauma, medication trauma, toxin exposures, or poor diet histories.

She points out EWG's work showing umbilical cord having 287 chemicals. Many of these are toxic to the brain and nervous system. Is there a correlation?

Or, could it have to do with the fact that women are having children in older age. We have to wonder if these toxins accumulate and end up in their babies' bodies.

"That's why I say that having a baby is one of the ways to detox because a lot of those toxins" are being transferred to the baby.

She says, the parents are "always hoping that their babies will outgrow all of this, which unfortunately" is not always the case.

"As a nutritionist, my role is to clean up the diet first and foremost. Then, heal the gut and support the detox pathways," she says.

Now, there's no statistically significance of the amount of GI issues in children with autism (77 percent) compared to those without autism (72 percent).

However, according to Brewster, what we need to question is why 72 to 77 percent of children are having GI issues in the first place?

Also, could there be correlations between autism and certain toxins like PPA (a preservative that crosses the blood-brain barrier)?

What about genetics, shares Brewster? There's no argument that autism is rising, but the CDC offers no explanation, except that genetic variations simply predispose for greater or lesser risk.

She then went on to show slides about the cycle of compromised immunity.

Previously, she shares, there has been research on children with autism and impaired detox pathways.

Now she's starting to get a little passionate in trying to convince us all that although there's controversy, we need to be open-minded to the anectodal evidence that nutritionists can share about relationship to diet.

She starts talking about "dysbiosis" and "leaky gut" and other stuff. Is there a connection with autistic spectrum disorders?

It's worth looking at the gut. Is there constipation? Can a "little change" like diet and regularity have an effect?

Once we (as nutritionists) fix maldigestion, malabsorption, dysbiosis, and inflammation in the gut ("the fire within"), we're helping to heal the child.

---

I have to admit I raised my eyebrows a lot during this talk, but what the hell do I know?

How is the gut related to a neurological disease?

What toxins are coming out in detox? What do you mean by detox? Psyllium hulls? Milk thistle? for children?

What's the connection to probiotics?

Still, despite the weaknesses in the argument for diet's relationship to autism, I can understand parents' needs to do everything they can to help their children.

This was just Part 1 of this seminar. Maybe I will have more answers in Part 2.